USP7 Active Human Recombinant Protein
- Known as:
- USP7 Active Human Recombinant Protein
- Catalog number:
- 80395
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- BPS Bioscience
- Gene target:
- USP7 Active Human Recombinant Protein
Related genes to: USP7 Active Human Recombinant Protein
- Gene:
- USP7 NIH gene
- Name:
- ubiquitin specific peptidase 7
- Previous symbol:
- HAUSP
- Synonyms:
- -
- Chromosome:
- 16p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-12
- Date modifiied:
- 2017-01-04
Related products to: USP7 Active Human Recombinant Protein
Related articles to: USP7 Active Human Recombinant Protein
- Hutchinson‑Gilford progeria syndrome (HGPS) is a rare premature aging disorder caused by mutations in the LMNA gene. High mobility group A1 (HMGA1) exhibits differential expression patterns across aging models. However, its roles and mechanisms in aging remain unclear. Here, we show a positive correlation between HMGA1 and the heterochromatin protein HP1β in multiple tissues of Lmna, a classic genetic mouse model of HGPS to recapitulate typical premature aging features, and naturally aging mice, and HP1β was decreased in Hmga1 mice. We further demonstrate that HMGA1 mitigates HGPS cellular senescence in a HP1β-dependent manner. Multi-omics reveals that HP1β downregulates angiopoietin-like protein 2 (ANGPTL2) by reducing chromatin accessibility, thereby suppressing SASP factors, and thus, alleviating senescence. Furthermore, HMGA1 stabilizes HP1β by recruiting de-ubiquitinating enzyme USP7. Based on the binding region of HMGA1 with HP1β and USP7, we develop a unique HMGA1 peptide (UHP) that prevents HP1β degradation, thereby ameliorating HGPS cellular senescence and significantly extending the lifespan of Lmna mice. Our findings elucidate a critical HMGA1-HP1β axis in premature aging and suggest that therapeutic strategies based on UHP may hold promise for HGPS. - Source: PubMed
Publication date: 2026/08/19
Hu QianyingSun QianXiang WeifangZhou ZilongSun HongyanHu YueYang LiehaoWang ChenyuZhang FangqingCong YujiaZhang YuXiao YichuanCong Xianling - Dysregulation of Cyclin D1 (CCND1) is implicated in various cancers, but its specific contribution to glioma radioresistance and the associated regulatory mechanisms remain largely unexplored. This research aimed to elucidate the functional role and underlying mechanisms of CCND1 in glioma radioresistance. Our findings revealed that CCND1 is significantly upregulated in glioma tissues, which correlates with a poor prognosis. Furthermore, CCND1 knockdown inhibited proliferation, triggered apoptosis, and augmented radiosensitivity in glioma cells. Additionally, CCND1 depletion sensitized glioma cells to irradiation by driving ferroptosis, as indicated by elevated reactive oxygen species (ROS) production, lipid peroxidation, and intracellular Fe accumulation. Mechanistically, USP7 was identified to stabilize the CCND1 protein via K48-linked deubiquitination. Notably, the ectopic expression of USP7 reversed the impacts of CCND1 knockdown on radiosensitivity, ferroptosis, cellular proliferation, and apoptosis. Altogether, our data indicate that the stabilization of CCND1 mediated by USP7 promotes radioresistance in glioma by suppressing ferroptosis. Therefore, targeting USP7 may serve as a promising therapeutic approach to augment the efficacy of radiotherapy in glioma. - Source: PubMed
Zhuo YayuZhang ChenruiLi XiaoyuDu ZishuoRong YirenZhang DiMi HaijuanGu XiaoyuWang FengHan HaieWu JianliangSun Jianping - The efficacy of immune checkpoint blockade in triple-negative breast cancer (TNBC) is limited by poor CD8⁺ T cell infiltration. Here, we demonstrate that tumor-derived proprotein convertase subtilisin/kexin type 9 (PCSK9) drives CD8⁺ T cell exclusion, and we identify protein arginine methyltransferase 5 (PRMT5) as an important epigenetic regulator responsible for PCSK9 expression in TNBC. Mechanistically, we elucidate that PRMT5-mediated methylation of the chromobox homolog 8 (CBX8) facilitates its interaction with the deubiquitinase USP7, which removes K33-linked ubiquitination on CBX8. This post-translational modification modulates CBX8 function, enabling it to drive the transcriptional upregulation of key downstream targets PCSK9, which inhibits CD8 T cell infiltration, and LGR5, which enhances tumor stemness. Crucially, inhibition of PRMT5 profoundly sensitizes TNBC tumors to anti-PD-1 therapy in vivo. Our work unveils a novel epigenetic pathway orchestrated by PRMT5 that converges on the functional modulation of CBX8 to synchronously governs CD8⁺ T cell exclusion and tumor stemness, nominating PRMT5 inhibition as a compelling therapeutic strategy for combination immunotherapy in TNBC. - Source: PubMed
Publication date: 2026/09/14
Chen CongcongZhang YuhengLiu ChangZhao RunkaiLiu KaimingGuo ZhiqiYang YinyinWang CongTian JiaxinGuo YanguanChen GuoJin LiyanZhu XunZhou DanyangJiang Guoqin - Non-small cell lung cancer (NSCLC) is a malignant tumor with high morbidity and mortality. Given the reported associations of both SET domain bifurcated histone lysine methyltransferase 1 (SETDB1) with various cancers and ubiquitin-specific protease 7 (USP7) with NSCLC progression, this study aims to elucidate the role of SETDB1 and USP7 in NSCLC progression. mRNA and protein levels were measured by qRT-PCR and Western blot, respectively. Cell biological phenotypes were evaluated using MTT, EdU, flow cytometry, transwell, and sphere formation assays. Ferroptosis was analyzed by measuring Fe2+, MDA GSH, and ROS levels. Relationship between USP7 and SETDB1 was examined through Co-IP, cycloheximide (CHX) chase, and deubiquitination assays. Xenograft tumor models were established to investigate the role of SETDB1 and USP7 in NSCLC in vivo. In NSCLC tissues and cells, SETDB1 levels were elevated. Knockdown of SETDB1 inhibited NSCLC cell viability, proliferation, invasion, and sphere formation ability, while promoting apoptosis and ferroptosis. Mechanistically, USP7 enhanced the stability of SETDB1 protein by its deubiquitination. USP7 knockdown suppressed NSCLC cell biological behavior by downregulating SETDB1. Moreover, USP7 knockdown repressed in vivo tumor growth of NSCLC. Taken together, USP7 suppresses ferroptosis and enhances growth in NSCLC cells by stabilizing SETDB1 protein through deubiquitination. - Source: PubMed
Zhang HongpeiFang YanfengWang XinxinWu WentingLi DandanZhang Yuan - Lactylation is an emerging post-translational modification that is well established for its involvement in epigenetic regulation. However, its functional significance and regulatory mechanisms in non-small cell lung cancer (NSCLC) remain poorly understood. In this study, integrated proteomic and lactylomic analyses of clinical NSCLC specimens and matched adjacent normal tissues showed that USP7 (ubiquitin specific peptidase 7) was upregulated and USP7 K1084 lactylation was increased in NSCLC. Knockout of or inhibition of USP7 lactylation impaired cellular mitophagy, resulting in mitochondrial damage and attenuated NSCLC tumorigenicity. We identified CREBBP/CBP (CREB binding lysine acetyltransferase) as the key lactyltransferase responsible for USP7 K1084 lactylation. USP7 lactylation induced its localization to mitochondria and increased its interaction with PINK1 (PTEN induced kinase 1), promoting PINK1 deubiquitination and stabilization. Pharmacological inhibition of CREBBP reduced USP7 lactylation levels and promoted PINK1 ubiquitination and degradation, exerting antitumor effects in vitro and in vivo. Analysis of NSCLC clinical specimens showed that the protein levels of USP7, CREBBP, and PINK1 were positively correlated, and their high expression was associated with poor patient prognosis. Collectively, our findings establish the CREBBP-USP7-PINK1 axis as a promising therapeutic target for NSCLC treatment.: CHX: cycloheximide; CREBBP/CBP: CREB binding lysine acetyltransferase; DUB: deubiquitinating enzyme; IHC: immunohistochemistry; IP: immunoprecipitation; KO: knockout; LDHA: lactate dehydrogenase A; MS: mass spectrometry; NALA: L-sodium lactate; NSCLC: non-small cell lung cancer; OCR: oxygen consumption rate; PBS: phosphate-buffered saline; PINK1: PTEN induced kinase 1; PLA: proximity ligation assay; ROS: reactive oxygen species; shRNA: short hairpin RNA; TEM: transmission electron microscopy; TUBE: tandem ubiquitin binding entity; UPS: ubiquitin-proteasome system; USP7: ubiquitin specific peptidase 7; WT: wild type. - Source: PubMed
Publication date: 2026/09/09
Wang ZhangjieLi ChaoyiZhu RuiqiuDuan MinghaoKuang ZhenyuLi XinCui WeifangDuan ChaojunZhang Chunfang